|
1
|
Van Damme P, Pintó RM, Feng Z, Cui F, Gentile A, Shouval D. Hepatitis A virus infection. Nat Rev Dis Primers 2023; 9:51. [PMID: 37770459 DOI: 10.1038/s41572-023-00461-2] [Citation(s) in RCA: 13] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 08/23/2023] [Indexed: 09/30/2023]
Abstract
Hepatitis A is a vaccine-preventable infection caused by the hepatitis A virus (HAV). Over 150 million new infections of hepatitis A occur annually. HAV causes an acute inflammatory reaction in the liver that usually resolves spontaneously without chronic sequelae. However, up to 20% of patients experience a prolonged or relapsed course and <1% experience acute liver failure. Host factors, such as immunological status, age, pregnancy and underlying hepatic diseases, can affect the severity of disease. Anti-HAV IgG antibodies produced in response to HAV infection persist for life and protect against re-infection; vaccine-induced antibodies against hepatitis A confer long-term protection. The WHO recommends vaccination for individuals at higher risk of infection and/or severe disease in countries with very low and low hepatitis A virus endemicity, and universal childhood vaccination in intermediate endemicity countries. To date, >25 countries worldwide have implemented such programmes, resulting in a reduction in the incidence of HAV infection. Improving hygiene and sanitation, rapid identification of outbreaks and fast and accurate intervention in outbreak control are essential to reducing HAV transmission.
Collapse
Affiliation(s)
- Pierre Van Damme
- Centre for the Evaluation of Vaccination, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
| | - Rosa M Pintó
- Department of Genetics, Microbiology and Statistics, Faculty of Biology, University of Barcelona, Barcelona, Spain
| | - Zongdi Feng
- Centre for Vaccines and Immunity, The Abigail Wexner Research Institute at Nationwide Children's Hospital, The Ohio State University College of Medicine, Columbus, OH, USA
| | - Fuqiang Cui
- Department of Laboratorial Science and Technology & Vaccine Research Center, School of Public Health, Peking University, Beijing, People's Republic of China
| | - Angela Gentile
- Department of Epidemiology, Hospital de Niños Ricardo Gutierrez, University of Buenos Aires, Buenos Aires, Argentina
| | - Daniel Shouval
- Institute of Hepatology, Hadassah-Hebrew University Hospital, Jerusalem, Israel
| |
Collapse
|
|
2
|
Sarma MS, Ravindranath A. Pediatric acute viral hepatitis with atypical variants: Clinical dilemmas and natural history. World J Hepatol 2022; 14:944-955. [PMID: 35721282 PMCID: PMC9157701 DOI: 10.4254/wjh.v14.i5.944] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/06/2022] [Revised: 02/20/2022] [Accepted: 05/07/2022] [Indexed: 02/06/2023] Open
Abstract
Classical acute viral hepatitis (AVH) has an uncomplicated outcome. Acute liver failure has a grave prognosis. Atypical manifestations of AVH are a group of disorders that causes significant morbidity and dilemmas in children. These include prolonged cholestasis, relapsing hepatitis, ascitic form of AVH, late-onset hepatic failure (LOHF), intravascular hemolysis, and provoking an autoimmune trigger leading to autoimmune hepatitis. These entities cause significant liver dysfunction or worsening and are often difficult to differentiate from chronic liver disease (CLD). Ascitic form of AVH, LOHF, decompensated CLD and acute-on-chronic liver failure have significant overlapping features that need to be carefully dissected out. In many cases, only on long-term follow-up, these clinical entities can be separately identified. Intravascular hemolysis is usually caused by associated glucose-6-phosphate dehydrogenase deficiency. Rarely CLD such as Wilson disease and autoimmune hepatitis can also present with hemolysis in the initial presentation, which can mimic AVH with hemolysis. Identifying deviations from typical manifestations aid in avoiding unnecessary investigations, allowing focused therapy and alleviating anxiety.
Collapse
Affiliation(s)
- Moinak Sen Sarma
- Department of Pediatric Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, Uttar Pradesh, India
| | - Aathira Ravindranath
- Division of Pediatric Gastroenterology, Apollo BGS Hospitals, Mysuru 570023, Karnataka, India
| |
Collapse
|
|
3
|
Ishizaka A, Koga M, Mizutani T, Lim LA, Adachi E, Ikeuchi K, Ueda R, Aoyagi H, Tanaka S, Kiyono H, Matano T, Aizaki H, Yoshio S, Mita E, Muramatsu M, Kanto T, Tsutsumi T, Yotsuyanagi H. Prolonged Gut Dysbiosis and Fecal Excretion of Hepatitis A Virus in Patients Infected with Human Immunodeficiency Virus. Viruses 2021; 13:v13102101. [PMID: 34696531 PMCID: PMC8539651 DOI: 10.3390/v13102101] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/17/2021] [Revised: 10/13/2021] [Accepted: 10/14/2021] [Indexed: 12/24/2022] Open
Abstract
Hepatitis A virus (HAV) causes transient acute infection, and little is known of viral shedding via the duodenum and into the intestinal environment, including the gut microbiome, from the period of infection until after the recovery of symptoms. Therefore, in this study, we aimed to comprehensively observe the amount of virus excreted into the intestinal tract, the changes in the intestinal microbiome, and the level of inflammation during the healing process. We used blood and stool specimens from patients with human immunodeficiency virus who were infected with HAV during the HAV outbreak in Japan in 2018. Moreover, we observed changes in fecal HAV RNA and quantified the plasma cytokine level and gut microbiome by 16S rRNA analysis from clinical onset to at least 6 months after healing. HAV was detected from clinical onset up to a period of more than 150 days. Immediately after infection, many pro-inflammatory cytokines were elicited, and some cytokines showed different behaviors. The intestinal microbiome changed significantly after infection (dysbiosis), and the dysbiosis continued for a long time after healing. These observations suggest that the immunocompromised state is associated with prolonged viral shedding into the intestinal tract and delayed recovery of the intestinal environment.
Collapse
Affiliation(s)
- Aya Ishizaka
- Division of Infectious Diseases, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (A.I.); (M.K.); (T.T.)
- International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan;
- Japan Foundation for AIDS Prevention, Tokyo 101-0064, Japan
| | - Michiko Koga
- Division of Infectious Diseases, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (A.I.); (M.K.); (T.T.)
| | - Taketoshi Mizutani
- Division of Infectious Diseases, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (A.I.); (M.K.); (T.T.)
- International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan;
- Correspondence: (T.M.); (H.Y.)
| | - Lay Ahyoung Lim
- Department of Infectious Diseases and Applied Immunology, IMSUT Hospital of Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (L.A.L.); (E.A.); (K.I.)
| | - Eisuke Adachi
- Department of Infectious Diseases and Applied Immunology, IMSUT Hospital of Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (L.A.L.); (E.A.); (K.I.)
| | - Kazuhiko Ikeuchi
- Department of Infectious Diseases and Applied Immunology, IMSUT Hospital of Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (L.A.L.); (E.A.); (K.I.)
| | - Ryuta Ueda
- Department of Virology II, National Institute of Infectious Diseases, Tokyo 162-8640, Japan; (R.U.); (H.A.); (H.A.); (M.M.)
| | - Haruyo Aoyagi
- Department of Virology II, National Institute of Infectious Diseases, Tokyo 162-8640, Japan; (R.U.); (H.A.); (H.A.); (M.M.)
| | - Satoshi Tanaka
- Department of Gastroenterology and Hepatology, National Hospital Organization Osaka National Hospital, Osaka 540-0006, Japan; (S.T.); (E.M.)
| | - Hiroshi Kiyono
- International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan;
- CU-UCSD Center for Mucosal Immunology, Allergy and Vaccines (cMAV), Department of Medicine, University of California San Diego, San Diego, CA 92093, USA
| | - Tetsuro Matano
- AIDS Research Center, National Institute of Infectious Diseases, Tokyo 162-8640, Japan;
- Department of AIDS Vaccine Development, IMSUT Hospital, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
| | - Hideki Aizaki
- Department of Virology II, National Institute of Infectious Diseases, Tokyo 162-8640, Japan; (R.U.); (H.A.); (H.A.); (M.M.)
| | - Sachiyo Yoshio
- The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Chiba 272-8516, Japan; (S.Y.); (T.K.)
| | - Eiji Mita
- Department of Gastroenterology and Hepatology, National Hospital Organization Osaka National Hospital, Osaka 540-0006, Japan; (S.T.); (E.M.)
| | - Masamichi Muramatsu
- Department of Virology II, National Institute of Infectious Diseases, Tokyo 162-8640, Japan; (R.U.); (H.A.); (H.A.); (M.M.)
| | - Tatsuya Kanto
- The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Chiba 272-8516, Japan; (S.Y.); (T.K.)
| | - Takeya Tsutsumi
- Division of Infectious Diseases, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (A.I.); (M.K.); (T.T.)
| | - Hiroshi Yotsuyanagi
- Division of Infectious Diseases, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (A.I.); (M.K.); (T.T.)
- Department of Infectious Diseases and Applied Immunology, IMSUT Hospital of Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan; (L.A.L.); (E.A.); (K.I.)
- Correspondence: (T.M.); (H.Y.)
| |
Collapse
|
|
4
|
Wang M, Feng Z. Mechanisms of Hepatocellular Injury in Hepatitis A. Viruses 2021; 13:v13050861. [PMID: 34066709 PMCID: PMC8151331 DOI: 10.3390/v13050861] [Citation(s) in RCA: 14] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2021] [Revised: 05/06/2021] [Accepted: 05/06/2021] [Indexed: 02/07/2023] Open
Abstract
Hepatitis A virus (HAV) infection is a common cause of acute viral hepatitis worldwide. Despite decades of research, the pathogenic mechanisms of hepatitis A remain incompletely understood. As the replication of HAV is noncytopathic in vitro, a widely accepted concept has been that virus-specific cytotoxic T cells are responsible for liver injury. However, accumulating evidence suggests that natural killer (NK) cells, NKT cells, and even non-HAV-specific CD8+ T cells contribute to liver damage during HAV infection. In addition, intrinsic death of virus-infected hepatocytes has been implicated as a cause of liver injury in a murine model of hepatitis A. Furthermore, genetic variations in host factors such as T cell immunoglobulin-1 (TIM1) and IL-18 binding protein (IL-18BP) have been linked to hepatitis A severity. This review summarizes the current knowledge of the mechanisms of hepatocellular injury in hepatitis A. Different mechanisms may be involved under different conditions and they are not necessarily mutually exclusive. A better understanding of these mechanisms would aid in diagnosis and treatment of diseases associated with HAV infection.
Collapse
Affiliation(s)
- Minghang Wang
- Center for Vaccines and Immunity, The Abigail Wexner Research Institute at Nationwide Children’s Hospital, Columbus, OH 43205, USA;
| | - Zongdi Feng
- Center for Vaccines and Immunity, The Abigail Wexner Research Institute at Nationwide Children’s Hospital, Columbus, OH 43205, USA;
- Department of Pediatrics, The Ohio State University College of Medicine, Columbus, OH 43210, USA
- Correspondence:
| |
Collapse
|
|
5
|
Walker CM. Adaptive Immune Responses in Hepatitis A Virus and Hepatitis E Virus Infections. Cold Spring Harb Perspect Med 2019; 9:cshperspect.a033472. [PMID: 29844218 DOI: 10.1101/cshperspect.a033472] [Citation(s) in RCA: 35] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
Both hepatitis A virus (HAV) and hepatitis E virus (HEV) cause self-limited infections in humans that are preventable by vaccination. Progress in characterizing adaptive immune responses against these enteric hepatitis viruses, and how they contribute to resolution of infection or liver injury, has therefore remained largely frozen for the past two decades. How HAV and HEV infections are so effectively controlled by B- and T-cell immunity, and why they do not have the same propensity to persist as HBV and HCV infections, cannot yet be adequately explained. The objective of this review is to summarize our understanding of the relationship between patterns of virus replication, adaptive immune responses, and acute liver injury in HAV and HEV infections. Gaps in knowledge, and recent studies that challenge long-held concepts of how antibodies and T cells contribute to control and pathogenesis of HAV and HEV infections, are highlighted.
Collapse
Affiliation(s)
- Christopher M Walker
- Center for Vaccines and Immunity, The Research Institute at Nationwide Children's, Columbus, Ohio 43004
| |
Collapse
|
|
6
|
Muñoz-Martínez SG, Díaz-Hernández HA, Suárez-Flores D, Sánchez-Ávila JF, Gamboa-Domínguez A, García-Juárez I, Torre A. Atypical manifestations of hepatitis A virus infection. REVISTA DE GASTROENTEROLOGÍA DE MÉXICO 2018; 83:134-143. [PMID: 29685743 DOI: 10.1016/j.rgmx.2017.10.004] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/12/2017] [Revised: 09/13/2017] [Accepted: 10/05/2017] [Indexed: 02/07/2023]
Abstract
Acute hepatitis due to the hepatitis A virus usually has a short, benign and self-limited course, without causing chronic hepatitis. However, some cases have an atypical presentation, such as relapsing hepatitis, prolonged or persistent cholestasis, fulminant hepatic failure, or liver failure associated with autoimmune hepatitis. The typical clinical course of acute hepatitis A virus infection is spontaneous remission in 90% of the cases, but atypical cases have a prevalence that varies from less than 1 to 20%, depending on the manifestation (overall prevalence ∼7%). There is little information on the atypical clinical courses of hepatitis A virus infection and the lack of recognizing those presentations in clinical practice often results in carrying out numerous studies and treatments that not only are unnecessary, but can also be harmful. The aim of the present article was to describe 3 clinical cases of atypical hepatitis A infection and provide a literature review of such cases.
Collapse
Affiliation(s)
- S G Muñoz-Martínez
- Departamento de Gastroenterología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
| | - H A Díaz-Hernández
- Departamento de Gastroenterología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
| | - D Suárez-Flores
- Departamento de Anatomía Patológica, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
| | - J F Sánchez-Ávila
- Departamento de Gastroenterología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México; Unidad de Hepatología y Trasplante hepático, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
| | - A Gamboa-Domínguez
- Departamento de Anatomía Patológica, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
| | - I García-Juárez
- Departamento de Gastroenterología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México; Unidad de Hepatología y Trasplante hepático, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
| | - A Torre
- Departamento de Gastroenterología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México; Unidad de Hepatología y Trasplante hepático, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México.
| |
Collapse
|
|
7
|
|
|
8
|
Foster MA, Weil LM, Jin S, Johnson T, Hayden-Mixson TR, Khudyakov Y, Annambhotla PD, Basavaraju SV, Kamili S, Ritter JM, Nelson N, Mazariegos G, Green M, Himes RW, Kuhar DT, Kuehnert MJ, Miller JA, Wiseman R, Moorman AC. Transmission of Hepatitis A Virus through Combined Liver-Small Intestine-Pancreas Transplantation. Emerg Infect Dis 2018; 23:590-596. [PMID: 28322704 PMCID: PMC5367420 DOI: 10.3201/eid2304.161532] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/19/2022] Open
Abstract
Vaccination of the donor might have prevented infection in the recipient and subsequent transmission to healthcare workers. Although transmission of hepatitis A virus (HAV) through blood transfusion has been documented, transmission through organ transplantation has not been reported. In August 2015, state health officials in Texas, USA, were notified of 2 home health nurses with HAV infection whose only common exposure was a child who had undergone multi–visceral organ transplantation 9 months earlier. Specimens from the nurses, organ donor, and all organ recipients were tested and medical records reviewed to determine a possible infection source. Identical HAV RNA sequences were detected from the serum of both nurses and the organ donor, as well as from the multi–visceral organ recipient’s serum and feces; this recipient’s posttransplant liver and intestine biopsy specimens also had detectable virus. The other organ recipients tested negative for HAV RNA. Vaccination of the donor might have prevented infection in the recipient and subsequent transmission to the healthcare workers.
Collapse
|
|
9
|
A Recombinant HAV Expressing a Neutralization Epitope of HEV Induces Immune Response against HAV and HEV in Mice. Viruses 2017; 9:v9090260. [PMID: 28914805 PMCID: PMC5618026 DOI: 10.3390/v9090260] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/22/2017] [Revised: 09/03/2017] [Accepted: 09/09/2017] [Indexed: 01/29/2023] Open
Abstract
Hepatitis A virus (HAV) and hepatitis E virus (HEV) are causative agents of acute viral hepatitis transmitted via the fecal–oral route. Both viruses place a heavy burden on the public health and economy of developing countries. To test the possibility that HAV could be used as an expression vector for the development of a combination vaccine against hepatitis A and E infections, recombinant HAV-HEp148 was created as a vector to express an HEV neutralization epitope (HEp148) located at aa 459–606 of the HEV capsid protein. The recombinant virus expressed the HEp148 protein in a partially dimerized state in HAV-susceptible cells. Immunization with the HAV-HEp148 virus induced a strong HAV- and HEV-specific immune response in mice. Thus, the present study demonstrates a novel approach to the development of a combined hepatitis A and E vaccine.
Collapse
|
|
10
|
Phylogenetic analysis of a transfusion-transmitted hepatitis A outbreak. Virus Genes 2016; 53:15-20. [PMID: 27660174 DOI: 10.1007/s11262-016-1392-0] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/28/2016] [Accepted: 09/19/2016] [Indexed: 10/21/2022]
Abstract
A transfusion-associated hepatitis A outbreak was found in the first time in Hungary. The outbreak involved five cases. Parenteral transmission of hepatitis A is rare, but may occur during viraemia. Direct sequencing of nested PCR products was performed, and all the examined samples were identical in the VP1/2A region of the hepatitis A virus genome. HAV sequences found in recent years were compared and phylogenetic analysis showed that the strain which caused these cases is the same as that had spread in Hungary recently causing several hepatitis A outbreaks throughout the country.
Collapse
|
|
11
|
Specific IgA Enhances the Transcytosis and Excretion of Hepatitis A Virus. Sci Rep 2016; 6:21855. [PMID: 26911447 PMCID: PMC4766440 DOI: 10.1038/srep21855] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/21/2015] [Accepted: 02/02/2016] [Indexed: 12/23/2022] Open
Abstract
Hepatitis A virus (HAV) replicates in the liver, and is excreted from the body in feces. However, the mechanisms of HAV transport from hepatocytes to the gastrointestinal tract are poorly understood, mainly due to lack of suitable in vitro models. Here, we use a polarized hepatic cell line and in vivo models to demonstrate vectorial transport of HAV from hepatocytes into bile via the apical cell membrane. Although this transport is specific for HAV, the rate of fecal excretion in inefficient, accounting for less than 1% of input virus from the bloodstream per hour. However, we also found that the rate of HAV excretion was enhanced in the presence of HAV-specific IgA. Using mice lacking the polymeric IgA receptor (pIgR−/−), we show that a proportion of HAV:IgA complexes are transported via the pIgR demonstrating a role for specific antibody in pathogen excretion.
Collapse
|
|
12
|
Abstract
Hepatitis A virus (HAV) is a faeco-orally transmitted picornavirus and is one of the main causes of acute hepatitis worldwide. An overview of the molecular biology of HAV is presented with an emphasis on recent findings. Immune evasion strategies and a possible correlation between HAV and atopy are discussed as well. Despite the availability of efficient vaccines, antiviral drugs targeting HAV are required to treat severe cases of fulminant hepatitis, contain outbreaks, and halt the potential spread of vaccine-escape variants. Additionally, such drugs could be used to shorten the period of illness and decrease associated economical costs. Several known inhibitors of HAV with various mechanisms of action will be discussed. Since none of these molecules is readily useable in the clinic and since the availability of an anti-HAV drug would be of clinical importance, increased efforts should be targeted toward discovery and development of such antivirals.
Collapse
Affiliation(s)
- Yannick Debing
- Rega Institute for Medical ResearchUniversity of LeuvenLeuvenBelgium
| | - Johan Neyts
- Rega Institute for Medical ResearchUniversity of LeuvenLeuvenBelgium
| | | |
Collapse
|
|
13
|
Weilandt R, Paulmann D, Schlottau K, Vallbracht A, Dotzauer A. Mutational modifications of hepatitis A virus proteins 2B and 2C described for cell culture-adapted and attenuated virus are present in wild-type virus populations. Arch Virol 2014; 159:2699-704. [DOI: 10.1007/s00705-014-2103-6] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2014] [Accepted: 04/25/2014] [Indexed: 01/27/2023]
|
|
14
|
Dotzauer A, Kraemer L. Innate and adaptive immune responses against picornaviruses and their counteractions: An overview. World J Virol 2012; 1:91-107. [PMID: 24175214 PMCID: PMC3782268 DOI: 10.5501/wjv.v1.i3.91] [Citation(s) in RCA: 29] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/08/2011] [Revised: 02/22/2012] [Accepted: 05/20/2012] [Indexed: 02/05/2023] Open
Abstract
Picornaviruses, small positive-stranded RNA viruses, cause a wide range of diseases which is based on their differential tissue and cell type tropisms. This diversity is reflected by the immune responses, both innate and adaptive, induced after infection, and the subsequent interactions of the viruses with the immune system. The defense mechanisms of the host and the countermeasures of the virus significantly contribute to the pathogenesis of the infections. Important human pathogens are poliovirus, coxsackievirus, human rhinovirus and hepatitis A virus. These viruses are the best-studied members of the family, and in this review we want to present the major aspects of the reciprocal effects between the immune system and these viruses.
Collapse
Affiliation(s)
- Andreas Dotzauer
- Andreas Dotzauer, Leena Kraemer, Department of Virology, University of Bremen, 28359 Bremen, Germany
| | | |
Collapse
|